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Phase 4 - Endo, Resp, Cardio, Haem, Opthal > Endocrine and Metabolic > Flashcards

Endocrine and Metabolic Flashcards

1
Q

How does acromegaly arise?

A

–> Excess growth hormone secondary to pituitary adenoma - 95%
–> Ectopic GHRH or GH production by tumours

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2
Q

What are the clinical features of acromegaly?

A

SPACE OCCUPYING PITUITARY TUMOUR
–> Headaches
–> Visual field defect (bitemporal hemianopia)

Excess growth hormone causes tissue growth:
–> Prominent forehead and brow (frontal bossing)
–> Coarse, sweaty skin
–> Large nose
–> Large tongue (macroglossia)
–> Large hands and feet
–> Large protruding jaw (prognathism)

Additional features include:
–> Hypertrophic heart
–> Hypertension
–> Type 2 diabetes
–> Carpal tunnel syndrome
–> Arthritis
–> Colorectal cancer

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3
Q

What are the investigations for acromegaly?

A

–> Insulin-like growth factor-1 (IGF-1). It indicates the growth hormone level and is raised in acromegaly.

–> Testing growth hormone directly is unreliable as it fluctuates throughout the day.

–> The growth hormone suppression test involves consuming a 75g glucose drink with growth hormone tested at baseline and 2 hours following the drink. The glucose should suppress the growth hormone level. Failure to suppress growth hormone indicates acromegaly.

–> MRI of the pituitary is used to diagnose a pituitary adenoma, although it may be too small to see on the scan.

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4
Q

What is the treatment for acromegaly?

A

–> Trans-sphenoidal surgery, to remove the pituitary tumour is the definitive treatment of acromegaly secondary to pituitary adenomas. Where acromegaly is caused by ectopic hormones from pancreatic or lung cancer, treatment ideally involves surgical removal of these tumours.

–> Radiotherapy may be used as part of treatment.

–> Medical options for reducing growth hormone are used in patients where surgery is not suitable:

Pegvisomant is a growth hormone receptor antagonist given daily by a subcutaneous injection
Somatostatin analogues (e.g., octreotide) block growth hormone release
Dopamine agonists (e.g., bromocriptine) block growth hormone release

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5
Q

What is Conns syndrome ?

A

–> Adrenal adenoma producing too much aldosterone

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6
Q

What is the presentation of hyperaldosteronism?

A

–> hypertension
–> hypokalaemia
–> alkalosis

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7
Q

What is the RAAS system?

A

–> Renin enzyme secreted by juxtaglomerular cells in afferent arteriole of kidney
–> renin secreted in response to hypotension
–> renin converts angiotensinogen (released by the liver) into angiotensin 1
–> Angiotensin 1 converts to angiotensin 2 in the lungs with the help of ACE
–> Angiotensin 2 stimulates the release of aldosterone from the adrenal glands
–> Aldosterone is a mineralocorticoid steroid hormone that increases sodium absorption, potassium secretion, increases hydrogen secretion

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8
Q

What is primary hyperaldosteronism?

A

–> Adrenal glands directly responsible for producing too much aldosterone, serum renin will be low as the high blood pressure suppresses it

–> could be caused by
Bilateral adrenal hyperplasia (most common)
Adrenal adenoma - Conns syndrome
Familial hyperaldosteronism

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9
Q

What is secondary hyperaldosteronsim?

A

–> Excessive renin stimulating release of excessive aldosterone

–> Due to disproportionately lower blood pressure in the kidneys - Renal artery stenosis/ heart failure/ liver cirrhosis and ascites

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10
Q

What are the investigations for hyperaldosteronism?

A

–> Aldosterone to renin ratio ARR
- high aldosterone low renin - primary hyperaldosteronism
- high aldosterone high renin - secondary hyperaldosteronism
–> raised blood pressure, low potassium, blood gas analysis
–> CT/MRI looking for a adrenal tumour or adrenal hyperplasia
–> renal artery imaging - for renal stenosis (Doppler, CT angiogram)
–> Adrenal vein sampling - to locate which gland is producing more aldosterone

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11
Q

What is the management of hyperaldosteronism?

A

Medical management is with aldosterone antagonists:

Eplerenone
Spironolactone

Treating the underlying cause involves:

Surgical removal of the adrenal adenoma
Percutaneous renal artery angioplasty via the femoral artery to treat renal artery stenosis

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12
Q

What is Cushings syndrome?

A

–> prolonged high levels of glucocorticoids in the body eg cortisol

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13
Q

What is Cushings disease?

A

–> Pituitary adenoma - secreting excessive ACTH - stimulating excessive cortisol release from the adrenal glands

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14
Q

What are the features of Cushings syndrome?

A

–> Round face (known as a “moon face”)
–> Central obesity
–> Abdominal striae (stretch marks)
–> Enlarged fat pad on the upper back (known as a “buffalo hump”)
–> Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
–> Male pattern facial hair in women (hirsutism)
–> Easy bruising and poor skin healing
–> Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)

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15
Q

What are the metabolic effects of Cushings syndrome?

A

–> Hypertension
–> Cardiac hypertrophy
–> type 2 diabetes
–> Dyslipidaemia
–> osteoporosis

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16
Q

What are the mental health effects of Cushings syndrome?

A

Mental health effects:

Anxiety
Depression
Insomnia
Rarely psychosis

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17
Q

What are the causes of Cushings syndrome?

A

C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome - ectopic ACTH
E – Exogenous steroids (patients taking long-term corticosteroids)

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18
Q

What tests or investigations can be carried out for Cushings syndrome/disease?

A

–> Dexamethasone suppression test
–> Full blood count may show a high white blood cell count
–> U&Es may show low potassium if an adrenal adenoma is also secreting aldosterone
–> MRI brain for a pituitary adenoma
–> CT chest for small cell lung cancer
–> CT abdomen for adrenal tumours

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19
Q

What are the key purposes and types of dexamethasone suppression tests in diagnosing Cushing’s syndrome?

A

–> Purpose: Diagnose Cushing’s syndrome caused by endogenous factors, not exogenous steroids.
–> Normal Response: Dexamethasone suppresses cortisol by negative feedback on the hypothalamus (↓CRH) and pituitary (↓ACTH).
–> Abnormal Response: Lack of cortisol suppression indicates Cushing’s syndrome.

Types of Tests:

Low-dose Overnight Test:
1mg dexamethasone at night.
Normal: Suppressed cortisol in the morning.
Abnormal: No suppression suggests Cushing’s.

Low-dose 48-hour Test:
0.5mg every 6 hours for 48 hours.
Normal: Suppressed cortisol on day 3.
Abnormal: No suppression suggests Cushing’s.

High-dose 48-hour Test:
2mg every 6 hours for 48 hours.
Cushing’s Disease: Cortisol suppression (pituitary adenoma).
Adrenal/Ectopic Tumors: No suppression.

ACTH Levels:
Low: Adrenal tumor (or exogenous steroids).
High: Pituitary tumor or ectopic ACTH (e.g., small cell lung cancer).

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20
Q

What is the treatment for Cushing’s disease?

A

The primary treatment is to remove the underlying cause:

–> Trans-sphenoidal (through the nose) removal of pituitary adenoma
–> Surgical removal of adrenal tumour
–> Surgical removal of the tumour producing ectopic ACTH (e.g., small cell lung cancer), if possible

Where surgical removal of the cause is not possible, another option is to surgically remove both adrenal glands (adrenalectomy) and give the patient life-long steroid replacement therapy.

Metyrapone reduces the production of cortisol in the adrenals and is occasionally used in treating of Cushing’s

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21
Q

What is Nelson’s syndrome and what does it cause?

A

Nelson’s syndrome involves the development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback. It causes skin pigmentation (high ACTH), bitemporal hemianopia and a lack of other pituitary hormones.

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22
Q

Why does diabetes insipidus occur?

A

–> A lack of antidiuretic hormone (cranial diabetes insipidus)
–> A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)

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23
Q

What is nephrogenic diabetes insipidus and what can it be caused by?

A

Nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH. It can be idiopathic, without a clear cause, or it can be caused by:

Medications, particularly lithium (used in bipolar affective disorder)
Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)
Hypercalcaemia (high calcium)
Hypokalaemia (low potassium)
Kidney diseases (e.g., polycystic kidney disease)

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24
Q

What is cranial diabetes insipidus and what can it be caused by?

A

Cranial diabetes insipidus is when the hypothalamus does not produce ADH for the pituitary gland to secrete. It can be idiopathic, without a clear cause, or it can be caused by:

Brain tumours
Brain injury
Brain surgery
Brain infections (e.g., meningitis or encephalitis)
Genetic mutations in the ADH gene (autosomal dominant inheritance)
Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)

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25
Q

What is the presentation of diabetes insipidus?

A

–> Polyuria (producing more than 3 litres of urine per day)
–> Polydipsia (excessive thirst)
–> Dehydration
–> Postural hypotension

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26
Q

What are the investigations for diabetes insipidus?

A

–> The water deprivation test is the test of choice for diagnosing diabetes insipidus.
–> Low urine osmolality (lots of water diluting the urine)
–> High/normal serum osmolality (water loss may be balanced by increased intake)
–> More than 3 liters on a 24-hour urine collection

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27
Q

How does the water deprivation test differentiate between primary polydipsia, cranial diabetes insipidus, and nephrogenic diabetes insipidus?

A

Procedure:
–> No fluids for up to 8 hours.
–> Measure urine osmolality after deprivation.
–> If low, administer desmopressin and measure urine osmolality over 2-4 hours.
Interpretation:

Primary Polydipsia:
–> High urine osmolality after water deprivation.
–> Desmopressin not needed.
–> Diagnosis: Rules out diabetes insipidus.

Cranial Diabetes Insipidus:
–> Low urine osmolality after water deprivation.
–> High urine osmolality after desmopressin.

Nephrogenic Diabetes Insipidus:
–> Low urine osmolality both before and after desmopressin.

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28
Q

What is the management of diabetes insipidus?

A

The underlying cause should be treated (e.g., stopping lithium). Mild cases may be managed conservatively.

Desmopressin (synthetic ADH) can be used in cranial diabetes insipidus to replace the absent antidiuretic hormone. The serum sodium needs to be monitored, as there is a risk of hyponatraemia (low sodium) with desmopressin.

Nephrogenic diabetes insipidus is less straightforward to treat. Management options include:

Ensuring access to plenty of water
High-dose desmopressin
Thiazide diuretics
NSAIDs

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29
Q

What is the cause of type 1 diabetes?

A

Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans of the pancreas. This process is thought to be influenced by a combination of genetic and environmental factors.

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30
Q

What is the pathophysiological process leading to Type 1 Diabetes Mellitus and its complications?

A

–> Mechanism: Type IV hypersensitivity autoimmune reaction where CD4+ T helper and CD8+ cytotoxic T cells attack pancreatic beta cells.
–> Progression: Beta cell destruction occurs over months to years, leading to hyperglycemia when ~90% of beta cells are destroyed.
–> Alpha Cell Dysfunction: Beta cell loss also affects alpha cells, causing excessive glucagon release, which leads to gluconeogenesis, glycogenolysis, and ketogenesis, worsening hyperglycemia and causing diabetic ketoacidosis.

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31
Q

What is the classic presentation of type 1 diabetes mellitus?

A

Typical Onset: Predominantly in childhood, most commonly diagnosed between ages 10-14.

Triad of Symptoms:

Polydipsia: Increased thirst due to hyperglycemia and fluid loss from polyuria.
Polyuria/Nocturia: Excessive urination due to renal glucose excretion and increased fluid intake.
Weight Loss: Loss of calories through glucose in urine.
Additional Symptoms:

Dry Mouth: Caused by dehydration from polyuria.
Lethargy: Due to lack of glucose uptake by cells.
Blurred Vision: Acute swelling of the lens from hyperglycemia.
Young Children: Symptoms may be hard to identify; look for Candida infections in the groin as a possible indicator.

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32
Q

What investigations confirm the diagnosis of diabetes mellitus?

A

–> Fasting blood glucose ≥7.0 mmol/L (≥126 mg/dL)
–> Non-fasting blood glucose ≥11.1 mmol/L (≥200 mg/dL)
–> Oral glucose tolerance test (OGTT): Blood glucose ≥11.1 mmol/L, 2 hours after 75 g glucose
–> HbA1c ≥48 mmol/mol (≥6.5%)

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33
Q

What investigations help identify Type 1 Diabetes Mellitus (T1DM)?

A

–> Autoantibodies (islet cells, IA2, GAD, ZnT8) indicate autoimmune beta cell destruction.
–> Fasting C-peptide is low or undetectable, indicating low endogenous insulin production.

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34
Q

What factors support a diagnosis of type 1 diabetes mellitus (T1DM)?

A

–> Age: Usually in childhood/adolescence
–> Clinical presentation: Polyuria, polydipsia, weight loss, lethargy, DKA
Ketosis: Often present, may lead to DKA
–> Autoantibodies: Islet cells, insulin, IA2, GAD, ZnT8
–> C-peptide: Low or undetectable (reflects low endogenous insulin production)

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35
Q

What are the key differences between Type 1 Diabetes Mellitus (T1DM) and Type 2 Diabetes Mellitus (T2DM)?

A

–> T2DM results from insulin resistance with relative insulin deficiency.
–> Slower onset and older age at diagnosis.
Ketosis uncommon.
–> Strong association with obesity and family history of T2DM.
–> Negative autoantibodies.
–> May respond to oral anti-hyperglycaemic drugs.

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36
Q

What are some causes of drug-induced diabetes

A

Prolonged use of corticosteroids, tacrolimus, L-asparaginase, or antipsychotics.

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37
Q

Name diseases of the exocrine pancreas that can cause diabetes.

A

Cystic fibrosis, chronic pancreatitis, hereditary haemochromatosis.

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38
Q

What are the key genetic and environmental factors contributing to Type 2 Diabetes Mellitus (T2DM)?

A

Genetic factors: Over 100 susceptibility loci identified by GWAS, involved in insulin secretion, action, and glucose metabolism.
Environmental factors: Obesity, physical inactivity, and high-calorie diets increase risk; diets rich in fiber, whole grains, and unsaturated fats reduce it.
Age & ethnicity: Risk increases after age 45, and certain ethnic groups (African Americans, Hispanics, Asians, Native Americans) are at higher risk.

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39
Q

What are the key mechanisms involved in the pathogenesis of Type 2 Diabetes Mellitus (T2DM)

A

–> insulin resistance: Caused by increased free fatty acids, pro-inflammatory cytokines, ectopic fat deposition, and oxidative stress, leading to impaired glucose uptake and increased hepatic glucose production.
–> β-cell dysfunction: Results from glucotoxicity, lipotoxicity, chronic inflammation, and amyloid deposition, causing reduced insulin secretion and eventual β-cell failure.

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40
Q

What are the common presentations of Type 2 Diabetes Mellitus (T2DM)

A

–> Asymptomatic (70%): Diagnosed on routine screening with hyperglycemia (fasting glucose >6.9 mmol/L, HbA1c >48 mmol/mol).
–> Subacute: Polyuria, fatigue, blurred vision, polydipsia, weight loss, nocturia, pruritis vulvae/balanitis (Candida infections).
–> Acute: Rare presentation with hyperosmolar hyperglycemic state (HHS), severe dehydration, and marked hyperglycemia without ketoacidosis.
–> Complications: 25% present with microvascular complications (e.g., retinopathy, nephropathy) at diagnosis.

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41
Q

What are the diagnostic criteria for Type 2 Diabetes Mellitus (T2DM)?

A

Symptomatic:
Fasting glucose ≥7.0 mmol/L
Random glucose ≥11.1 mmol/L (or 2h post-75g glucose load)
Asymptomatic: Same criteria but must be confirmed on two occasions.
HbA1c: ≥48 mmol/mol (6.5%) is diagnostic, but repeat test required for asymptomatic patients.
Conditions where HbA1c is unreliable: Haemoglobinopathies, haemolytic anemia, untreated iron deficiency anemia, suspected gestational diabetes, children, HIV, chronic kidney disease, steroid use.

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42
Q

What are the criteria for impaired fasting glucose (IFG) and impaired glucose tolerance (IGT)?

A

–> Impaired Fasting Glucose (IFG): Fasting glucose ≥6.1 but <7.0 mmol/L.
–> Impaired Glucose Tolerance (IGT): Fasting glucose <7.0 mmol/L and 2-hour OGTT value ≥7.8 but <11.1 mmol/L.
–> Diabetes UK Guidance: For IFG, an OGTT should be performed. If the OGTT result is between 7.8 and 11.1 mmol/L, it confirms IGT, not diabetes.

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43
Q

What are the updated HbA1c targets for managing Type 2 Diabetes Mellitus (T2DM) according to NICE guidelines?

A

–> Lifestyle alone or lifestyle + metformin: HbA1c target is 48 mmol/mol (6.5%).

–> Lifestyle + drugs causing hypoglycemia (e.g., sulfonylureas): HbA1c target is 53 mmol/mol (7.0%).

–> If already on one drug and HbA1c rises to 58 mmol/mol (7.5%): Adjust target to 53 mmol/mol (7.0%).

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44
Q

What is the first-line treatment for Type 2 Diabetes Mellitus and how should it be managed?

A

–> Metformin: First-line drug; titrate slowly to minimize gastrointestinal issues. Use modified-release if standard-release is not tolerated.
–> If metformin is contraindicated: Use SGLT-2 inhibitors (if CVD risk, established CVD, or chronic heart failure), otherwise DPP-4 inhibitors, pioglitazone, or sulfonylureas.

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45
Q

What are the second-line and third-line treatment options if HbA1c targets are not met with initial therapy?

A

–> Second-line: Add one of the following to metformin: DPP-4 inhibitor, pioglitazone, sulfonylurea, or SGLT-2 inhibitor (if NICE criteria met).
–> Third-line: Add another drug or insulin if needed: metformin + DPP-4 inhibitor + sulfonylurea, or pioglitazone + sulfonylurea, or insulin.

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46
Q

What are the guidelines for starting and managing insulin therapy in T2DM?

A

Start insulin: Continue metformin; begin with human NPH insulin (intermediate-acting).
GLP-1 mimetics: Consider if BMI ≥35 kg/m² with obesity-related issues or if insulin therapy has significant implications. Continue only if HbA1c drops by at least 11 mmol/mol (1.0%) and weight loss is ≥3% in 6 months.

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47
Q

What are the recommended approaches for managing hypertension and lipids in T2DM patients?

A

–> Hypertension: Aim for clinic BP targets of 140/90 mmHg (age <80) or 150/90 mmHg (age >80). Use ACE inhibitors or ARBs; ARB preferred for black African or African-Caribbean origin.
–> Lipids: Statins recommended if 10-year cardiovascular risk >10%. First-line: atorvastatin 20 mg.

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48
Q

What is the mechanism of action of Metformin?

A

Increases insulin sensitivity and decreases liver glucose production.

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49
Q

What are notable side effects of Metformin?

A

Gastrointestinal issues (pain, nausea, diarrhea), and rare lactic acidosis (especially with acute kidney injury).

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50
Q

What should be done if a patient experiences gastrointestinal side effects with Metformin?

A

They can try modified-release Metformin.

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51
Q

What is the mechanism of action of SGLT-2 inhibitors?

A

Blocks glucose reabsorption in the kidneys, increasing glucose excretion in urine.

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52
Q

Name a few examples of SGLT-2 inhibitors.

A

Empagliflozin, Canagliflozin, Dapagliflozin, Ertugliflozin.

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53
Q

What are notable side effects of SGLT-2 inhibitors?

A

Glycosuria, increased urination, genital and urinary tract infections, weight loss, and rare Fournier’s gangrene and lower-limb amputation (more common with Canagliflozin).

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54
Q

What is the mechanism of action of Pioglitazone?

A

Increases insulin sensitivity and decreases liver glucose production.

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55
Q

What are notable side effects of Pioglitazone?

A

Weight gain, heart failure, increased risk of bone fractures, and a small increase in bladder cancer risk.

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56
Q

Give an example of sulfonylureas

A

Gliclazide

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57
Q

How do Sulfonylureas work in diabetes management?

A

Stimulate insulin release from the pancreas.

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58
Q

What are notable side effects of Sulfonylureas?

A

Weight gain and hypoglycemia.

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59
Q

What is the pathophysiology of Diabetic Ketoacidosis (DKA)?

A

–> Insulin Deficiency: Causes hyperglycemia, ketosis, and metabolic acidosis.
–> Hyperglycemia: Due to increased gluconeogenesis and glycogenolysis in the liver, and decreased glucose utilization in peripheral tissues.
–> Ketosis: Insulin deficiency leads to lipolysis, producing free fatty acids converted to ketone bodies (β-hydroxybutyrate and acetoacetate) in the liver.
–> Metabolic Acidosis: Accumulation of ketone bodies causes an anion gap metabolic acidosis.
–> Common Triggers: Infection, missed insulin doses, and myocardial infarction.

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60
Q

What do DPP-4 inhibitors do, and what are some examples?

A

DPP-4 inhibitors block the DPP-4 enzyme, increasing incretin activity. Examples include sitagliptin and alogliptin.

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61
Q

What is the onset and duration of rapid-acting insulin?

A

Rapid-acting insulin (e.g., NovoRapid) starts working in about 10 minutes and lasts for approximately 4 hours.

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62
Q

What is the mechanism of GLP-1 mimetics, and can you name a few examples?

A

GLP-1 mimetics imitate the action of GLP-1, increasing insulin secretion and slowing glucose absorption. Examples include exenatide and liraglutide.

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63
Q

What are the key presentation features of Diabetic Ketoacidosis (DKA)?

A

–> Triad: Hyperglycemia, ketosis, metabolic acidosis.
–> Hyperglycemia: Blood glucose >11 mmol/L, causing polyuria, polydipsia, blurred vision, headache, lethargy.
–> Acidosis: pH <7.3, bicarbonate <15 mmol/L; Kussmaul breathing (deep, rapid) to expel CO₂.
–> Ketosis: Sweet, fruity or acetone breath odor; due to increased ketone bodies.
–> Dehydration: Dry mucous membranes, tachycardia, hypotension, decreased skin turgor; electrolyte imbalances (e.g., hypokalemia).
–> Neurological Symptoms: Altered mental status, possible seizures.
–> Abdominal Symptoms: Pain, nausea, vomiting, can mimic acute abdomen.
–> Precipitating Factors: Infections, poor insulin compliance, newly diagnosed diabetes, myocardial infarction.

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64
Q

What are the diagnostic criteria for Diabetic Ketoacidosis (DKA) according to the Joint British Diabetes Societies (2013)?

A

Glucose: >11 mmol/L or known diabetes mellitus
pH: <7.3
Bicarbonate: <15 mmol/L
Ketones: >3 mmol/L or urine ketones ++ on dipstick

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65
Q

What are the main principles of managing Diabetic Ketoacidosis (DKA)?

A

–> Fluid Replacement:
Most patients are depleted by 5-8 liters.
Start with isotonic saline, even if acidotic.
Insulin: Begin intravenous infusion at 0.1 unit/kg/hour.
When glucose <14 mmol/L, add 10% dextrose at 125 mL/hr.

–> Electrolyte Correction:
Serum potassium often high initially but total body potassium is low.
Monitor and potentially add potassium to replacement fluids.
Cardiac monitoring required if potassium infusion >20 mmol/hour.

–> Insulin Management:
Continue long-acting insulin.
Discontinue short-acting insulin.

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66
Q

What are the complications of DKA and its treatment?

A

–> Gastric Stasis: Impaired gastric motility.
–> Thromboembolism: Increased risk of VTE due to dehydration and hypercoagulability; consider VTE prophylaxis.
–> Arrhythmias: Can be caused by hyperkalaemia or iatrogenic hypokalaemia.
–> Cerebral Oedema: Rare, particularly in children; manifests as headache, altered mental status, seizures. Usually occurs 4-12 hours after treatment starts. Seek CT head and senior review if suspected.
–> Acute Respiratory Distress Syndrome
–> Acute Kidney Injury
–> Hypoglycaemia and Hypokalaemia: Can occur due to incorrect fluid therapy.

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67
Q

What is the pathophysiology of Hyperosmolar Hyperglycemic State (HHS)?

A

–> Hyperglycaemia leads to osmotic diuresis, causing loss of sodium and potassium.
–> Severe Volume Depletion results in high serum osmolarity (>320 mosmol/kg) and hyperviscosity of blood.
–> Dehydration may be less apparent due to hypertonicity preserving intravascular volume.

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68
Q

What are the clinical features of Hyperosmolar Hyperglycemic State (HHS)?

A

–> General: Fatigue, lethargy, nausea, vomiting
–> Neurological: Altered level of consciousness, headaches, papilloedema, weakness
–> Haematological: Hyperviscosity (can cause myocardial infarctions, stroke, peripheral arterial thrombosis)
–> Cardiovascular: Dehydration, hypotension, tachycardia

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69
Q

What are the diagnostic criteria for Hyperosmolar Hyperglycemic State (HHS)?

A

–> Hypovolaemia
–> Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
–> Significantly Raised Serum Osmolarity (>320 mosmol/kg)

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70
Q

What are the main principles of managing Hyperosmolar Hyperglycemic State (HHS)?

A

–> Normalise Osmolality (Gradually):
Fluid losses in HHS are 100-220 ml/kg.
Use IV 0.9% sodium chloride initially.
Switch to 0.45% sodium chloride if osmolality doesn’t decline.
Aim to replace 50% of fluid loss in the first 12 hours and the remainder in the next 12 hours.
Avoid rapid changes in serum osmolarity; monitor hourly.
A safe reduction rate for blood glucose is 4-6 mmol/hr. Aim for a target of 10-15 mmol/L.
Complete normalization may take up to 72 hours.

–> Fluid Replacement:
Start with IV 0.9% sodium chloride, adjusting to 0.45% if needed.
Avoid rapid rehydration, especially in those with heart failure or chronic kidney disease.

–> Insulin:
Only start if significant ketonaemia is present (β-hydroxybutyrate >1 mmol/L).
Use IV insulin infusion at 0.05 units/kg/hr.
Avoid insulin if ketonaemia is not significant, as it can cause rapid osmolarity changes.

–> Electrolyte Correction:
Monitor and replace potassium as necessary.
Potassium levels can be affected by insulin and fluid replacement.
Cardiac monitoring is needed if potassium infusion exceeds 20 mmol/hr.

–> Monitoring Response:
Track serum osmolarity, sodium, and glucose levels.
A rise in serum sodium with decreasing glucose is expected but should be monitored.
Avoid a sodium rise greater than 2.4 mmol/L for each 5.5 mmol/L fall in glucose.

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71
Q

How long does short-acting insulin take to start working, and how long does it last?

A

Short-acting insulin (e.g., Actrapid) starts working in around 30 minutes and lasts about 8 hours.

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72
Q

What is the onset and duration of intermediate-acting insulin?

A

Intermediate-acting insulin (e.g., Humulin I) starts working in about 1 hour and lasts for around 16 hours.

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73
Q

What is the onset and duration of long-acting insulin?

A

Long-acting insulin (e.g., Levemir, Lantus) starts working in about 1 hour and lasts 24 hours or longer.

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74
Q

What are combination insulins, and can you name a few with their ratios?

A

Humalog 25: 25% rapid-acting, 75% intermediate-acting
Humalog 50: 50% rapid-acting, 50% intermediate-acting
Novomix 30: 30% rapid-acting, 70% intermediate-acting

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75
Q

How often should patients be screened for diabetic nephropathy using urinary albumin ratio (ACR)?

A

annual

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76
Q

When should the specimen for ACR testing be collected?

A

early morning

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77
Q

What ACR value indicates microalbuminuria?

A

An ACR greater than 2.5.

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78
Q

What is the primary dietary recommendation for managing diabetic nephropathy?

A

Dietary protein restriction.

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79
Q

What is the target blood pressure for managing diabetic nephropathy?

A

Less than 130/80 mmHg.

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80
Q

When should an ACE inhibitor or angiotensin-II receptor antagonist be started for diabetic nephropathy?

A

If urinary ACR is 3 mg/mmol or more.

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81
Q

What type of sensory loss is typical in diabetic peripheral neuropathy?

A

Sensory loss with a ‘glove and stocking’ distribution.

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82
Q

What is the first-line treatment for diabetic neuropathic pain according to NICE guidelines?

A

Amitriptyline, duloxetine, gabapentin, or pregabalin.

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83
Q

What can be used as ‘rescue therapy’ for exacerbations of neuropathic pain?

A

tramadol

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84
Q

What topical treatment is used for localized neuropathic pain?

A

Capsaicin

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85
Q

What is a common symptom of gastroparesis in diabetic autonomic neuropathy?

A

Erratic blood glucose control, bloating, and vomiting.

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86
Q

What prokinetic agents can be used to manage gastroparesis?

A

Metoclopramide, domperidone, or erythromycin.

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87
Q

What causes gastro-oesophageal reflux disease in diabetic autonomic neuropathy?

A

Decreased lower esophageal sphincter (LES) pressure.

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88
Q

Why does hyperkalaemia tend to be associated with acidosis?

A

Potassium and hydrogen ions compete; higher potassium levels reduce hydrogen ion entry into cells.

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89
Q

What conditions can cause hypokalaemia with alkalosis?

A

Vomiting
Thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism).

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90
Q

What conditions can cause hypokalaemia with acidosis?

A

RAPID mnemonic
Renal tubular acidosis
Acetazolamide
Partially treated diabetic ketoacidosis.
Diarrhoea

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91
Q

How can magnesium deficiency affect potassium levels?

A

It can cause hypokalaemia, and normalizing potassium levels may be difficult until magnesium deficiency is corrected.

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92
Q

What are the ECG features for hypokalaemia?

A

In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

U waves
No T waves or small
Long PR
Long QT
ST depression

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93
Q

What are the features of hypokalaemia?

A

–> muscle weakness, hypotonia
–> hypokalaemia predisposes patients to digoxin toxicity - care should be taken if patients are also on diuretics

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94
Q

Why is metabolic acidosis associated with hyperkalaemia?

A

Hydrogen and potassium ions compete for exchange with sodium ions across cell membranes and in the distal tubule.

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95
Q

What ECG changes are seen in hyperkalaemia?

A

Tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern, and asystole.

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96
Q

What are some common causes of hyperkalaemia?

A

RAAMMD mnemonic
Rhabdomyolysis
Acute kidney injury
Addison’s disease
Metabolic acidosis
Massive blood transfusion.
Drugs (potassium-sparing diuretics, ACE inhibitors, angiotensin II receptor blockers, spironolactone, ciclosporin, heparin)

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97
Q

What is the treatment of hypokalaemia?

A

Potassium chloride (oral)

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98
Q

How do beta-blockers and heparin affect potassium levels?

A

Beta-blockers interfere with potassium transport into cells, potentially causing hyperkalaemia in renal failure.

Both unfractionated and low-molecular weight heparin can cause hyperkalaemia by inhibiting aldosterone secretion.

99
Q

What are the stages of hyperkalaemia according to the European Resuscitation Council?

A

Mild: 5.5 - 5.9 mmol/L
Moderate: 6.0 - 6.4 mmol/L
Severe: ≥ 6.5 mmol/L

100
Q

What ECG changes are associated with hyperkalaemia?

A

Peaked or ‘tall-tented’ T waves
Loss of P waves
Broad QRS complexes
Sinusoidal wave pattern

101
Q

What are the principles of hyperkalaemia treatment?

A

Stabilisation of cardiac membrane: IV calcium gluconate (does NOT lower serum potassium).
Short-term shift of potassium: Insulin/dextrose infusion, nebulised salbutamol.
Removal of potassium: Calcium resonium (oral/enema), loop diuretics, dialysis, haemofiltration/haemodialysis for persistent hyperkalaemia with AKI.

102
Q

When do you treat hyperkalaemia

A

Treat the underlying cause if K+ is <6.5 and no ECG changes
IF ECG changes and >6.5 then treat with:
IV calcium gluconate
IV insulin and dextrose

103
Q

What is the immediate management for severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes?

A

IV calcium gluconate: To stabilise the myocardium.
Insulin/dextrose infusion: For short-term potassium shift from ECF to ICF.
Other treatments: Nebulised salbutamol for temporary reduction in serum potassium.

104
Q

What additional steps should be taken in the management of hyperkalaemia?

A

Stop exacerbating drugs: e.g., ACE inhibitors.
Treat underlying cause.
Lower total body potassium: Calcium resonium, loop diuretics, dialysis.

105
Q

What is primary hyperparathyroidism, and what is the most common cause?

A

–> Primary hyperparathyroidism is a condition of excess parathyroid hormone (PTH) secretion leading to hypercalcemia. —–> The most common cause is a solitary parathyroid adenoma (85%).

106
Q

What are the less common causes of primary hyperparathyroidism

A

Less common causes include hyperplasia (10%), multiple adenomas (4%), and parathyroid carcinoma (1%).

107
Q

What are the key risk factors for developing primary hyperparathyroidism?

A

–> Key risk factors include being female (women are 2-3 times more likely to develop it),
–> older age (most common between 55-75 years)
–> family history, which increases the risk of multi-gland disease and may suggest MEN.

108
Q

How does parathyroid hormone (PTH) normally regulate calcium homeostasis?

A

–> PTH is secreted in response to low serum calcium levels and acts on bones, kidneys, and indirectly the bowels to move calcium into the bloodstream, increasing calcium levels to the normal range. Once normal, PTH secretion decreases.

109
Q

How does primary hyperparathyroidism disrupt normal calcium homeostasis?

A

In primary hyperparathyroidism, certain parathyroid cells fail to respond to the negative feedback from normal calcium levels, continuously secreting PTH, leading to hypercalcemia.

110
Q

How are most patients with primary hyperparathyroidism identified?

A

–> Most patients are asymptomatic and are often identified incidentally through raised serum calcium levels discovered during unrelated investigations. They may report mild symptoms such as fatigue, weakness, depression, or cognitive impairment if questioned.

111
Q

What mnemonic helps remember the symptoms of hypercalcemia in primary hyperparathyroidism, and what does it stand for?

A

The mnemonic ‘stones, bones, abdominal groans, and psychic overtones’:

–> Stones: Increased risk of kidney stones (17%)
–> Bones: Bone pain (35%), osteopenia and osteoporosis (40%)
–> Abdominal groans: Abdominal pain, constipation, nausea, vomiting
–> Psychic overtones: Fatigue, depression (10%), memory impairment (18%)

112
Q

What other symptoms may occur as calcium levels rise in primary hyperparathyroidism?

A

Other symptoms include polyuria, paresthesia, muscle cramps, and, in severe cases, cardiac/metabolic disturbances, delirium, or coma.

113
Q

What should be assessed during the physical examination of a patient with primary hyperparathyroidism?

A

Assess fluid status (due to dehydration risk from polyuria and reduced intake), cognitive function (as hypercalcemia can mimic dementia or depression in the elderly), and screen for signs of malignancy through neck, respiratory, abdominal, breast, and lymphoreticular examinations.

114
Q

How is primary hyperparathyroidism diagnosed?

A

By measuring serum adjusted calcium and parathyroid hormone (PTH) levels simultaneously. Typically, both calcium and PTH are elevated, but a raised calcium with a normal PTH also suggests primary hyperparathyroidism due to inappropriately high PTH levels for the elevated calcium.

115
Q

What is considered hypercalcemia, and what are the typical findings in primary hyperparathyroidism?

A

Hypercalcemia is defined as serum adjusted calcium >2.6 mmol/L. Primary hyperparathyroidism usually progresses slowly and is mild. If clinical suspicion is high, high-normal calcium levels should be investigated further.

116
Q

What are the key findings on serum PTH in primary hyperparathyroidism?

A

PTH is raised in primary and tertiary hyperparathyroidism. An inappropriately normal PTH in the context of hypercalcemia is also indicative of the disease. Low PTH suggests malignancy or PTH-independent causes of hypercalcemia.

117
Q

What additional tests help differentiate primary hyperparathyroidism from other conditions?

A

24-hour urinary calcium: High-normal in primary hyperparathyroidism, low in familial hypocalciuric hypercalcemia.

eGFR and creatinine: To assess kidney function.
Serum/urine protein electrophoresis: To rule out myeloma.
Full blood count (FBC): To exclude hematological malignancies.
Liver function tests (LFTs): To rule out liver metastases and systemic diseases.
DEXA scan: To assess bone health and risk of osteopenia/osteoporosis.

118
Q

How are most patients with primary hyperparathyroidism managed initially?

A

They are usually managed by their GP and then referred to a surgeon for a parathyroidectomy.

119
Q

What do the 2019 NICE guidelines recommend regarding surgery for primary hyperparathyroidism?

A

Parathyroidectomy is recommended for most patients due to high cure rates (up to 98%) and fewer drug side effects.

120
Q

What are the indications for parathyroidectomy according to the 2019 NICE guidelines?

A

Symptomatic hypercalcemia
Osteoporosis or fragility fractures
Renal stones or nephrocalcinosis
Age <50 years
Serum adjusted calcium ≥2.85 mmol/L
eGFR <60 mL/min/1.73 m²

121
Q

What are the management options for patients who cannot undergo parathyroid surgery?

A

–> Calcitonin: Inhibits bone and kidney calcium resorption
–> Cinacalcet: Calcimimetic that lowers calcium without affecting bone density or urinary calcium
–> Denosumab: Inhibits calcium resorption
Bisphosphonates

122
Q

What is hypoparathyroidism?

A

Hypoparathyroidism is an endocrine disorder characterised by deficient or absent parathyroid hormone (PTH) production, resulting in low blood calcium levels and high phosphate levels

123
Q

What are the primary blood abnormalities in hypoparathyroidism?

A

Low calcium levels (hypocalcemia) and high phosphate levels (hyperphosphatemia).

124
Q

What are the common causes of hypoparathyroidism?

A

–> Post-surgical: Damage or removal of the parathyroid glands during neck surgery, especially thyroidectomy.
–> Autoimmune: Destruction of the parathyroid gland, often associated with polyglandular autoimmune syndromes.
–> Congenital: Genetic disorders like DiGeorge syndrome causing absent or malfunctioning glands.
–> Idiopathic: Unknown cause despite investigation.
–> -Metabolic/Nutritional: Prolonged hypomagnesemia or excessive iron/copper deposition (haemochromatosis, Wilson’s disease) damaging the glands.
–> Radiation: Damage from radiation therapy to the neck.

125
Q

How does hypoparathyroidism affect PTH’s role in calcium and phosphate regulation?

A

–> Reduced PTH Production: Leads to impaired regulation of calcium by acting on bones, kidneys, and intestines.
–> Bone Resorption: Less PTH reduces osteoclast activity, lowering calcium release from bones.
–> Renal Calcium Reabsorption: Without PTH, more calcium is lost in the urine, worsening hypocalcemia.
–> Vitamin D Metabolism: Reduced PTH decreases conversion of vitamin D to its active form (calcitriol), reducing calcium absorption from the intestines.
–> Phosphate Handling: PTH normally promotes phosphate excretion. Without it, phosphate retention occurs, reducing free calcium levels.

126
Q

What is the hallmark of hypoparathyroidism and what are its common symptoms?

A

–> The hallmark is hypocalcemia, presenting with neuromuscular irritability. –> Symptoms range from mild numbness/tingling, muscle cramps, and fatigue to severe manifestations like tetany, carpopedal spasm, laryngospasm, and seizures.

127
Q

What physical signs are associated with hypoparathyroidism?

A

Chvostek’s sign: Twitching of the facial muscles in response to tapping over the facial nerve.
Trousseau’s sign: Carpopedal spasm induced by occluding the brachial artery with a blood pressure cuff.

128
Q

What are some long-term complications of hypocalcemia in hypoparathyroidism?

A

Extrapyramidal symptoms
Cataracts
Calcification of the basal ganglia.

129
Q

How is hypoparathyroidism diagnosed?

A

Diagnosis is based on low serum calcium, low or inappropriately normal PTH levels, and hyperphosphatemia. Additionally, urinary calcium excretion may be low, and magnesium levels should be checked, especially if magnesium deficiency is suspected.

130
Q

What can an ECG reveal in a patient with hypoparathyroidism?

A

A prolonged QT interval due to hypocalcemia.

131
Q

What may radiographs show in patients with hypoparathyroidism?

A

Intracranial calcifications or changes in bone density.

132
Q

What is the primary goal of treating hypoparathyroidism?

A

To maintain a slightly low to low-normal serum calcium level to avoid hypercalciuria and renal complications.

133
Q

What are the main treatments for hypoparathyroidism?

A

Oral calcium supplements
Active vitamin D analogues: such as calcitriol or alfacalcidol

134
Q

What regular monitoring is required for patients with hypoparathyroidism?

A

Monitoring for symptoms of hypocalcemia and periodic checks of serum calcium, phosphate, magnesium levels, renal function, and urinary calcium excretion.

135
Q

What dietary modifications should be advised for patients with hypoparathyroidism?

A

A high-calcium, low-phosphorus diet.

136
Q

What are the features of hypercalcaemia?

A

–> ‘bones, stones, groans and psychic moans’
–> corneal calcification
–> shortened QT interval on ECG
–> hypertension

137
Q

What are the two conditions that account for 90% of cases of hypercalcemia?

A

–> Primary hyperparathyroidism: Most common in non-hospitalized patients.
–> Malignancy: Most common in hospitalized patients, including causes like PTHrP from tumors, bone metastases, and myeloma.

138
Q

What are some malignancy-related processes that can cause hypercalcemia?

A

–> PTHrP: Produced by tumors such as squamous cell lung cancer.
–> Bone metastases: Can lead to hypercalcemia.
–> Myeloma: Causes increased osteoclastic bone resorption due to cytokines like IL-1 and tumor necrosis factor.

139
Q

What is the key investigation for patients with hypercalcemia?

A

Measuring parathyroid hormone (PTH) levels.

140
Q

What are other causes of hypercalcemia beyond primary hyperparathyroidism and malignancy?

A

Drugs: thiazides, calcium-containing antacids
Sarcoidosis
Vitamin D intoxication
Granulomas (e.g., tuberculosis, histoplasmosis)
Acromegaly
Thyrotoxicosis
Milk-alkali syndrome
Dehydration
Addison’s disease
Paget’s disease of the bone: Hypercalcemia may occur with prolonged immobilization.

141
Q

What is the initial management for hypercalcemia?

A

Rehydration with normal saline, typically 3-4 liters per day.

142
Q

What are the treatments used after rehydration for managing hypercalcemia, and how long do they take to show effects?

A

–> Bisphosphonates: Take 2-3 days to start working, with maximal effect at 7 days.
–> Calcitonin: Provides a quicker effect than bisphosphonates.
–> Steroids: Used specifically for hypercalcemia due to sarcoidosis.

143
Q

When might loop diuretics such as furosemide be used in hypercalcemia, and what precautions should be taken?

A

Loop diuretics may be used if patients cannot tolerate aggressive fluid rehydration. They should be used with caution as they can worsen electrolyte derangement and volume depletion.

144
Q

What are the primary features of hypocalcemia?

A

Tetany: Muscle twitching, cramping, and spasm
Perioral paraesthesia: Tingling around the mouth
Chronic symptoms: Depression, cataracts
ECG: Prolonged QT interval

145
Q

What is Trousseau’s sign, and how is it elicited?

A

Definition: Carpal spasm induced by occluding the brachial artery with a blood pressure cuff.
Method: Inflate the cuff above systolic pressure and maintain it.
Appearance: Wrist flexion and fingers drawn together.
Prevalence: Seen in around 95% of patients with hypocalcemia and around 1% of normocalcemic people.

146
Q

What is Chvostek’s sign, and how is it tested?

A

Definition: Facial muscle twitching in response to tapping over the parotid gland.
Prevalence: Seen in around 70% of patients with hypocalcemia and around 10% of normocalcemic people.

147
Q

What are the common causes of hypocalcemia?

A

Vitamin D deficiency (e.g., osteomalacia)
Chronic kidney disease
Hypoparathyroidism (e.g., post thyroid/parathyroid surgery)
Pseudohypoparathyroidism (target cells insensitive to PTH)
Rhabdomyolysis (initial stages)
Magnesium deficiency (due to end-organ PTH resistance)
Massive blood transfusion
Acute pancreatitis
Contamination: Blood samples contaminated with EDTA can cause falsely low calcium levels.

148
Q

How is severe hypocalcemia managed?

A

–> Intravenous calcium replacement: Preferred method is intravenous calcium gluconate, 10 ml of 10% solution over 10 minutes.
–> Alternative: Intravenous calcium chloride, though more likely to cause local irritation.
–> Monitoring: ECG monitoring is recommended during treatment.
Further management: Depends on the underlying cause of hypocalcemia.

149
Q

What is hypothermia and how is it defined?

A

Hypothermia is an unintentional reduction in core body temperature below normal physiological limits.

Mild hypothermia: 32-35°C
Moderate or severe hypothermia: < 32°C

150
Q

What are the common causes of hypothermia?

A

Exposure to cold in the environment
Inadequate insulation in the operating room
Cardiopulmonary bypass
Newborn babies

151
Q

What are the risk factors for hypothermia?

A

General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age

152
Q

What are the signs and symptoms of hypothermia?

A

Mild: Shivering, cold and pale skin, slurred speech, tachypnoea, tachycardia, hypertension
Moderate: Respiratory depression, bradycardia, hypotension, confusion/impaired mental state
Severe: Severe confusion, impaired mental status, potential cardiac arrest

153
Q

What investigations should be conducted for a patient with hypothermia?

A

Temperature (low-reading rectal thermometers or thermistor probes)
12-lead ECG (look for ST-elevation and J waves)
FBC and serum electrolytes
Blood glucose
Arterial blood gas
Coagulation factors
Chest X-ray

154
Q

What is the initial management of hypothermia?

A

Remove from the cold environment and wet/cold clothing
Warm with blankets
Secure airway and monitor breathing
If needed, use warm IV fluids or forced warm air
Be prepared for CPR if severe; avoid IV drugs if possible

155
Q

What should NOT be done when managing a person with hypothermia?

A

Do not put them into a hot bath
Do not massage their limbs
Do not use heating lamps
Do not give them alcohol to drink

156
Q

What ECG changes may be seen in hypothermia?

A

bradycardia
‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias

157
Q

What are some causes of hypoglycemia?

A

–> Insulinoma: Increased ratio of proinsulin to insulin
–> Self-administration of insulin/sulphonylureas
–> Liver failure
–> Addison’s disease
–> Alcohol: Increases insulin secretion due to effects on pancreatic blood flow
–> Nesidioblastosis: Beta cell hyperplasia

158
Q

What are the physiological responses to hypoglycemia?

A

Hormonal Response: Decreased insulin secretion, increased glucagon, later increased growth hormone and cortisol
Sympathoadrenal Response: Increased catecholamine (adrenergic) and acetylcholine (cholinergic) neurotransmission

159
Q

What are the symptoms of hypoglycemia at different blood glucose levels?

A

<3.3 mmol/L: Autonomic symptoms (sweating, shaking, hunger, anxiety, nausea)
<2.8 mmol/L: Neuroglycopenic symptoms (weakness, vision changes, confusion, dizziness)
Severe/Uncommon Features: Convulsion, coma

160
Q

What is the management of hypoglycemia in the community?

A

Initial Treatment: Oral glucose (10-20g in liquid, gel, or tablet form)
Alternatives: Quick-acting carbohydrate (e.g., GlucoGel, Dextrogel)
For severe cases: HypoKit containing glucagon for IM or SC injection

161
Q

What is the management of hypoglycemia in a hospital setting?

A

If Alert: Quick-acting carbohydrate (glucogel/dextrogel)
If Unconscious or Unable to Swallow:
Glucagon: Subcutaneous or intramuscular injection
Alternatively: Intravenous 20% glucose solution through a large vein

162
Q

What is the prevalence of hypothyroidism in the UK and its gender distribution?

A

Hypothyroidism affects around 1-2% of women in the UK and is 5-10 times more common in females than males.

163
Q

What are the primary causes of hypothyroidism?

A

–> Hashimoto’s Thyroiditis: Most common cause, an autoimmune disease, often associated with IDDM, Addison’s disease, or pernicious anemia; may cause transient thyrotoxicosis in acute phase
–> Subacute Thyroiditis (de Quervain’s): Inflammatory condition
–> Riedel Thyroiditis: Fibrous thyroiditis
–> Post-Thyroidectomy or Radioiodine Treatment: Removal or destruction of thyroid tissue
–>Drug Therapy: Lithium, amiodarone, anti-thyroid drugs (e.g., carbimazole)
–>Dietary Iodine Deficiency: Lack of iodine in the diet

164
Q

What are some conditions associated with hypothyroidism?

A

Down’s Syndrome
Turner’s Syndrome
Coeliac Disease

165
Q

What are the general symptoms of hypothyroidism?

A

Weight gain
Lethargy
Cold intolerance

166
Q

What skin changes are associated with hypothyroidism?

A

Dry (anhydrosis), cold, yellowish skin
Non-pitting oedema (e.g., hands, face)
Dry, coarse scalp hair
Loss of lateral aspect of eyebrows

167
Q

What gastrointestinal symptoms are seen in hypothyroidism?

A

Constipation

168
Q

What are the gynaecological features of hypothyroidism?

A

Menorrhagia

169
Q

What neurological signs are associated with hypothyroidism?

A

Decreased deep tendon reflexes
Carpal tunnel syndrome

170
Q

What other occasional symptom may be noted in hypothyroidism?

A

Hoarse voice

171
Q

What are the key points in the management of hypothyroidism with levothyroxine therapy?

A

–>Initial Dosage:
Elderly patients and those with ischemic heart disease: Start with 25 mcg daily, slowly titrate.
Other patients: Start with 50-100 mcg daily.

–> Monitoring:
Check thyroid function tests 8-12 weeks after changing the levothyroxine dose.
Aim for a TSH level in the range of 0.5-2.5 mU/L.

–>Pregnancy:
Increase levothyroxine dose by 25-50 mcg for pregnant women with established hypothyroidism.
Monitor TSH carefully during pregnancy, aiming for a low-normal value.

172
Q

What are the side effects of levothyroxine therapy?

A

–>Side Effects:
Over-treatment can lead to hyperthyroidism, reduced bone mineral density, worsening angina, and atrial fibrillation.

173
Q

What drug interacts with levothyroxine?

A

–> Drug Interactions:
Iron reduces levothyroxine absorption; take them at least 2 hours apart.

174
Q

How is Body Mass Index (BMI) classified?

A

Underweight: < 18.49 kg/m²
Normal: 18.5 - 25 kg/m²
Overweight: 25 - 30 kg/m²
Obese Class 1: 30 - 35 kg/m²
Obese Class 2: 35 - 40 kg/m²
Obese Class 3: > 40 kg/m²

175
Q

What are the steps in the management of obesity?

A

–> Conservative: Diet and exercise
–> Medical - Orlistat: A pancreatic lipase inhibitor
Liraglutide: A GLP-1 mimetic
–> Surgical: Reserved for specific cases of severe obesity

176
Q

What are the criteria for prescribing Orlistat in obesity management?

A

BMI of ≥ 28 kg/m² with associated risk factors (T2DM, hypertension or hypercholesterolaemia), or
BMI of ≥ 30 kg/m²
Only be continued if weight loss (e.g. ≥ 5% after 3 months)
Usually prescribed for < 1 year

177
Q

What are the criteria for using Liraglutide in obesity management?

A

BMI ≥ 35 kg/m²
Prediabetic hyperglycaemia (e.g., HbA1c 42 - 47 mmol/mol)
Administered as a daily subcutaneous injection

178
Q

What is osteoporosis?

A

Osteoporosis is a complex, progressive skeletal disease characterized by reduced bone mineral density and defects in bone tissue micro-architecture, leading to an increased risk of fragility fractures.

179
Q

What are the primary forms of osteoporosis?

A

Postmenopausal osteoporosis (Type I): Linked to decreased estrogen levels.
Age-related osteoporosis (Type II): Occurs naturally with aging

180
Q

What are the causes of secondary osteoporosis?

A

Hyperthyroidism
Hyperparathyroidism
Alcohol abuse
Immobilisation

181
Q

Why is osteoporosis more common in women than men?

A

Men generally have greater bone mass at any age and do not experience a menopause equivalent, while post-menopausal women face increased bone tissue degradation due to decreased estrogen levels.

182
Q

What are the main management options for osteoporosis?

A

Oral bisphosphonates
Lifestyle modification: Exercise and vitamin D supplements
Monoclonal antibody treatment (for some patients to prevent further reduction in bone mineral density)

183
Q

What are the two main determinants of bone strength?

A

Bone density: Amount of bone present.
Bone quality: Trabeculization of bone.

184
Q

What tool is commonly used to assess fracture risk in patients with osteoporosis?

A

The FRAX tool is used to calculate the 10-year risk of a major osteoporotic fracture and a hip fracture, based on various risk factors.

185
Q

What are the major risk factors for osteoporotic fractures according to the FRAX tool?

A

Age (between 40 and 90 years)
Gender
Previous fracture
Parent with fractured hip
Smoking
Glucocorticoid use (>3 months at a dose of prednisolone 5mg daily)
Rheumatoid arthritis
Secondary osteoporosis
Alcohol consumption
Bone Mineral Density (BMD)

186
Q

Which patients does NICE recommend assessing for osteoporosis?

A

Anyone on long-term oral corticosteroids or with a previous fragility fracture
Anyone >= 50 with risk factors
All women over 65
All men over 75

187
Q

How does long-term glucocorticoid use increase the risk of osteoporotic fractures?

A

Taking glucocorticoids for more than 3 months, especially at doses of prednisolone 5mg daily or higher, is associated with increased bone loss, raising the risk of fractures.

188
Q

How do different factors like oestrogen deficiency, glucocorticoid use, and ageing affect bone micro-architecture and remodelling in osteoporosis?

A

–> Oestrogen deficiency:
Increased number of remodelling units.
Premature arrest of osteoblasts, leading to perforation of trabeculae.
Loss of fracture resistance.

–> Glucocorticoids:
Initial phase: High-turnover state with increased fracture risk within 3 months.
Prolonged use: Reduced bone synthesis by osteoblasts, leading to net bone loss. Common with prednisolone doses of 10mg daily for 3 months or more.

–> Ageing:
Increased bone turnover at the bone/vascular interface in cortical bone, leading to trabeculization of cortical bone and weak long bone structure.

189
Q

How does osteoporosis typically present, and what are the most common pathological fractures associated with it?

A

–> Typical presentation:
Osteoporosis often remains asymptomatic during its latent period, with fragility fractures being the first clinical sign. These occur most frequently in older women, with a sharp increase in prevalence from 2% at 50 years to 25% by 80 years.

Common pathological fractures:
–> Vertebral compression fractures:
Acute back pain, worsened by prolonged standing or bending.
Thoracic kyphosis (Dowager’s hump) from anterior compression fractures.
Only 1 in 3 vertebral fractures are symptomatic.
–> Appendicular fractures:
Proximal femur (hip): Hip pain, inability to bear weight, shortened and externally rotated leg.
Distal radius (Colles): Wrist pain and reduced movement after a fall on an outstretched hand.
Complications:
–> Post-operative recovery often complicated by co-morbidities (e.g., pneumonia, DVT).

190
Q

What is the diagnostic work-up for osteoporosis, and how is bone mineral density measured and interpreted?

A

–> Evaluate bone density loss.
–> Exclude secondary causes of bone loss.
–> Monitor therapy/preventative intervention effectiveness.

Bone mineral density measurement:
Dual-energy X-ray absorptiometry (DXA): Measures bone mineral density using low radiation.
T-score interpretation:
-1.0 = Normal.
-1.0 to -2.5 = Osteopenia.
< -2.5 = Osteoporosis.
Secondary cause investigations:

Quantitative CT/US of heel.
Lab tests: FBC, U&Es, LFTs, TFTs, 25-OH vitamin D, testosterone.
Radiographs: Lumbar/thoracic spine for fractures.
Additional: Protein electrophoresis, urinary Bence-Jones protein.

191
Q

How does osteomalacia differ from osteoporosis in terms of bone mineral density and symptoms?

A

–> Osteoporosis: Decreased density of normally mineralized bone matrix, often asymptomatic until fractures occur.
–> Osteomalacia: Insufficient bone mineralization; may have variable BMD, causes generalized bone pain, tenderness, and myopathy.

192
Q

What is the key difference between Paget disease of bone and osteoporosis?

A

–> Osteoporosis: Decreased bone mass with normal bone structure, increased fracture risk.
–> Paget Disease: Excessive osteoclastic bone resorption and compensatory osteoblast formation. New bone is weaker (mosaic pattern), leading to deformities, bone and joint pain, and neurological complications.

193
Q

What laboratory findings help differentiate osteoporosis, osteomalacia, and Paget disease?

A

–> Osteoporosis: Normal serum calcium, phosphate, alkaline phosphatase (ALP), and parathyroid hormone (PTH).
–> Osteomalacia: Decreased serum calcium and phosphate, increased ALP and PTH.
–> Paget Disease: Normal serum calcium and phosphate, increased ALP, normal PTH.

194
Q

Which secondary causes of osteoporosis should be considered in differential diagnosis?

A

Hyperparathyroidism.
Mastocytosis.
Sickle cell anemia.
Myeloma and other neoplastic bone diseases (e.g., primary or metastatic tumors, lymphoma).

195
Q

What are the diagnostic investigations and management options for osteoporosis?

A

–> Falls risk assessment
–> Weight-bearing and muscle strengthening exercises
–> Ensure daily intake of calcium (800-1200mg) and vitamin D (400-800 IU)
–> Calculate 10-year fracture risk (FRAX)

–> Lifestyle Modification:
Encourage exercise and sufficient vitamin D and calcium intake.

–> Pharmacological Therapy:
Oral bisphosphonates (Alendronate or Risedronate) for high fracture risk (>1% on FRAX).
Denosumab for extensive osteoporosis (subcutaneous injection every 6 months).
Hormone Replacement Therapy (HRT) for early postmenopausal women (reserved use due to breast cancer and cardiovascular risks).

–> Specific Treatments:
Glucocorticoid-Induced Osteoporosis: Start bone-protection at glucocorticoid therapy onset.
Osteoporosis in Men: Bisphosphonates first-line, Denosumab alternative for those intolerant.

–> Fracture Management:
Bed rest, strong analgesia, and physiotherapy for vertebral fractures.

196
Q

What causes osteomalacia?

A

Osteomalacia is caused by a deficiency of vitamin D, leading to softening and weakening of bones.

197
Q

What is the treatment for osteomalacia?

A

–> High doses of vitamin D supplements
–> Calcium supplements
–> Lifestyle changes like increased sun exposure and dietary modifications

198
Q

What are the musculoskeletal symptoms, skeletal deformities, neurological, and extra-skeletal manifestations of osteomalacia?

A

Musculoskeletal Symptoms:

Bone pain: Diffuse, poorly localized, typically affecting lower back, hips, pelvis, and lower extremities.
Muscle weakness: Proximal weakness, especially in lower limbs, causing difficulty climbing stairs or walking.
Joint pain: Arthralgia, especially in large joints like hips and shoulders.
Fractures: Insufficiency fractures from minimal trauma or spontaneously.
Skeletal Deformities:

Pseudofractures (Looser’s zones): Radiolucent bands indicating unmineralized osteoid.
Bowing deformities: Seen in long bones such as femur and tibia.
Spinal deformities: Vertebral compression fractures may cause kyphosis or scoliosis.

Neurological Manifestations:
Paresthesia: Numbness or tingling in extremities due to hypocalcemia.
Tetany: Carpopedal spasm, Chvostek’s or Trousseau’s sign due to severe hypocalcemia.
Extra-skeletal Manifestations:

Dental abnormalities: Dental caries, enamel hypoplasia, and periodontal disease.

Nonspecific symptoms: Fatigue, anorexia, and weight loss.

199
Q

How are pituitary adenomas classified?

A

By Size:
–> Microadenoma: <1cm
–> Macroadenoma: ≥1cm
By Hormonal Status:
–> Secretory/Functioning: Produces excess hormones
–> Non-Secretory/Non-Functioning: Does not produce excess hormones

200
Q

What are the common types of pituitary adenomas?

A

–> Prolactinomas (most common): Excess prolactin production
–> Non-Secreting Adenomas
–> Growth Hormone (GH) Secreting Adenomas: Cause acromegaly
–> Adrenocorticotropic Hormone (ACTH) Secreting Adenomas: Cause Cushing’s disease

201
Q

What symptoms do pituitary adenomas cause?

A

–> Hormonal excess: Cushing’s disease (ACTH), acromegaly (GH), amenorrhea and galactorrhea (prolactin)
–> Hormonal deficiency: Generalized hypopituitarism
–> Dura stretching: Headaches
–> Optic chiasm compression: Bitemporal hemianopia

202
Q

What investigations are required for diagnosing pituitary adenomas?

A

–> Pituitary blood profile (GH, prolactin, ACTH, FSH, LSH, TFTs)
–> Formal visual field testing
–> MRI brain with contrast

203
Q

What are the differential diagnoses for a pituitary adenoma?

A

Pituitary hyperplasia
Craniopharyngioma
Meningioma
Brain metastases
Lymphoma
Hypophysitis
Vascular malformation (e.g., aneurysm)

204
Q

What are the treatment options for pituitary adenomas?

A

–> Medical Therapy:
Prolactinomas: Dopamine agonists (cabergoline, bromocriptine)
GH-secreting adenomas: Somatostatin analogues, GH receptor antagonists
ACTH-secreting adenomas: Cortisol synthesis inhibitors, neuromodulators
–> Surgery: Transsphenoidal surgery (primary treatment)
–> Radiotherapy: For residual or recurrent tumors after surgery

205
Q

What is Syndrome of Inappropriate ADH Secretion (SIADH) characterized by?

A

SIADH is characterized by hyponatraemia due to the dilutional effects of excessive water retention, with patients typically being euvolemic, meaning they do not show signs of overt volume depletion or overload.

206
Q

What is the pathophysiology of SIADH?

A

–> Excessive ADH (vasopressin) release leads to water retention, volume expansion, and dilutional hyponatraemia.
–> ADH increases water reabsorption in kidney collecting ducts, decreasing urine output.
–> In SIADH, ADH release continues despite normal/excess body fluid levels, leading to excessive water retention without signs of fluid overload (e.g., oedema, hypertension).
–> Dilution of electrolytes, especially sodium, causes hyponatraemia.

207
Q

What are the causes of SIADH?

A

Malignancy:
–> Small cell lung cancer
Also: pancreas, prostate cancers

Neurological:
–> Stroke, subarachnoid/subdural haemorrhage
–> Meningitis, encephalitis, abscess

Infections:
–> Tuberculosis
–> Pneumonia

Drugs:
–> Sulfonylureas, SSRIs, tricyclics
–> Carbamazepine, vincristine, –> cyclophosphamide

Other Causes:
Positive end-expiratory pressure (PEEP)
Porphyrias

MOST IMPORTANT TO REMEMBER: 2S2P mnemonic
SSRIs
Small cell lung cancer
Pneumonia
Post-surgery

208
Q

What are the symptoms of SIADH?

A

Headache
Fatigue
Muscle aches and cramps
Confusion

209
Q

What investigations are used in SIADH diagnosis?

A

–> Urine osmolality: Inappropriately high (>100 mOsm/kg), as urine should be more diluted with low serum osmolality.
–> Urine sodium concentration: Typically high (>40 mmol/L) due to ADH’s effect on renal tubules.

210
Q

How is SIADH managed?

A

–> Slow correction of hyponatraemia: To avoid central pontine myelinolysis.
–> Fluid restriction.
–> Demeclocycline: Reduces responsiveness of renal tubule cells to ADH.
–> ADH receptor antagonists may also be used.

211
Q

What is thyroid eye disease (Graves’ ophthalmopathy)?

A

It is an autoimmune disorder where immune cells infiltrate the extraocular muscles and orbital connective tissues, leading to inflammation, oedema, and fibrosis, which can cause proptosis, diplopia, restrictive strabismus, exposure keratopathy, and potentially compressive optic neuropathy.

212
Q

What are the clinical manifestations of thyroid eye disease?

A

Mild: Eyelid retraction.
Severe: Proptosis, diplopia, restrictive strabismus, exposure keratopathy, and sight-threatening compressive optic neuropathy.

213
Q

How is thyroid eye disease assessed?

A

Clinical examination: Signs like lid lag or Von Graefe’s sign.
Imaging: CT or MRI orbits to assess muscle involvement.
Serological tests: For thyroid function.

214
Q

What are the management strategies for thyroid eye disease?

A

Medical: Corticosteroids are the first-line treatment during the active phase to reduce inflammation.
Surgical: Orbital decompression surgery may be necessary for optic nerve compression or severe proptosis causing corneal breakdown.

215
Q

What are the key features of thyroid eye disease?

A

–> Exophthalmos (proptosis or bulging eyes)
–> Conjunctival oedema
–> Optic disc swelling
–> Ophthalmoplegia (restricted eye movement)

216
Q

What are the risks associated with an inability to close the eyelids in thyroid eye disease?

A

Sore, dry eyes due to exposure.
If severe and untreated, patients are at risk of exposure keratopathy.

217
Q

What is the first-line management for corneal protection in thyroid eye disease?

A

Topical lubricants are used to prevent corneal inflammation caused by exposure.

218
Q

What role do steroids play in managing thyroid eye disease?

A

Steroids are used to reduce inflammation, particularly during the active phase of the disease.

219
Q

What other treatments may be used in thyroid eye disease management?

A

Radiotherapy: May be used to reduce inflammation.
Surgery: Indicated for severe cases, such as optic nerve compression or significant proptosis.

220
Q

What are common benign causes of thyroid nodules?

A

Multinodular goitre
Thyroid adenoma
Hashimoto’s thyroiditis
Cysts (colloid, simple, or hemorrhagic)

221
Q

What are common malignant causes of thyroid nodules?

A

Papillary carcinoma (most common malignant cause)
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
Lymphoma

222
Q

What are the main investigations for thyroid nodules?

A

Thyroid function tests should be done in all patients.
Ultrasonography is the first-line imaging to assess for features suspicious of malignancy.

223
Q

What are the general features of thyrotoxicosis?

A

Weight loss
Feeling “manic” or restless
Heat intolerance

224
Q

What are the cardiac features of thyrotoxicosis?

A

Palpitations and tachycardia
High-output cardiac failure, especially in elderly patients
Rarely, reversible cardiomyopathy

225
Q

What are the skin features of thyrotoxicosis?

A

Increased sweating
Pretibial myxoedema: erythematous, oedematous lesions above the lateral malleoli
Thyroid acropachy: clubbing

226
Q

What is the primary gastrointestinal feature of thyrotoxicosis?

A

Diarrhoea

227
Q

What is the primary gynaecological feature of thyrotoxicosis?

A

Oligomenorrhea (infrequent menstrual periods)

228
Q

What are the neurological features of thyrotoxicosis?

A

Anxiety
Tremor

229
Q

What is Graves’ disease?

A

Graves’ disease is an autoimmune condition where antibodies form against thyroid-stimulating hormone (TSH), leading to overproduction of thyroid hormones. It is the most common cause of hyperthyroidism in developed countries.

230
Q

What autoimmune diseases are commonly associated with Graves’ disease?

A

–> Type 1 diabetes mellitus
–> Addison’s disease
–> Pernicious anaemia

231
Q

What type of hypersensitivity reaction is involved in Graves’ disease?

A

Graves’ disease involves a type II hypersensitivity reaction, where IgG antibodies bind to TSH receptors on thyroid follicular cells, causing chronic stimulation.

232
Q

What effects result from chronic stimulation of the TSH receptor in Graves’ disease?

A

Chronic stimulation of the TSH receptor in Graves’ disease results in:

Excessive production of thyroid hormones (T3 and T4)
Hypertrophy of the thyroid gland
Hyperplasia of thyroid follicular cells
Signs and symptoms of hyperthyroidism and goitre

233
Q

What are the metabolic signs and symptoms of hyperthyroidism in Graves’ disease?

A

Heat intolerance: Increased metabolism raises body temperature.
Weight loss: Due to a higher metabolic rate.
Increased appetite: Seen in 90% of patients, usually without weight gain.
Excessive sweating: Must be differentiated from post-menopausal hot flushes.

234
Q

What cardiac symptoms are associated with hyperthyroidism in Graves’ disease?

A

Palpitations: Including atrial fibrillation or other supraventricular tachycardias, especially in older patients.
Tachycardia
Atrial fibrillation
Hypertension
Heart failure: Thyrotoxic cardiomyopathy, particularly in the elderly.

235
Q

What are the symptoms related to excessive nervous stimulation in Graves’ disease?

A

Anxiety: Feeling of nervousness and trembling.
Tremor: Typically fine.

236
Q

What are the thyroid-related features of hyperthyroidism in Graves’ disease?

A

Palpable thyroid: Smooth, diffusely and uniformly enlarged goitre.
Oligomenorrhoea

237
Q

What extrathyroidal manifestations are specific to Graves’ disease?

A

Eye disease (30%): Includes upper eyelid retraction, exophthalmos, ophthalmoplegia, eye pain, tearing, diplopia, photophobia, and blurred vision.
Pretibial myxoedema (3%): Waxy, discoloured induration on the anterior lower legs.
Thyroid acropachy (1%): Clubbing of fingers and toes, with soft tissue swelling due to sub-periosteal bone formation.

238
Q

What are the NICE 2019 guideline recommendations for step 1 in testing for thyroid dysfunction?

A

Step 1: Test for thyroid dysfunction.
Tests include:
TSH: Low in hyperthyroidism.
Free thyroxine (fT4): High in hyperthyroidism.
Free triiodothyronine (fT3): High in hyperthyroidism.
Consider repeating tests if symptoms worsen or new symptoms develop (at least 6 weeks after the previous test).

239
Q

What is the second step in testing for hyperthyroidism according to the NICE 2019 guidelines?

A

Step 2: If hyperthyroidism is confirmed, test for Graves’ disease.
Specific tests for Graves’ disease:
TSH receptor antibodies (TRAbs): Present in Graves’ disease with a sensitivity >97% and specificity >98%.
Technetium scan: Considered if TRAbs are negative.

240
Q

What imaging options does NICE recommend for hyperthyroidism?

A

–> Imaging is considered if a discrete thyroid nodule is palpated.

Options include:
Ultrasound scan: Assesses size, vascularity, and nodules (enlarged, hypervascular thyroid with nodules in ~15% of Graves’ patients).

Radioactive iodine scan:
Diffuse and high uptake: Suggests Graves’.
Uneven uptake: Indicates a nodule.
Low uptake: Suggests thyroiditis.

241
Q

How is thyroid eye disease assessed?

A

Examine visual fields, acuity, and eye movements.
MRI or CT scans: Can confirm diagnosis, especially in subclinical cases.

242
Q

How are cardiac complications in Graves’ disease assessed?

A

Perform an ECG to assess for potential cardiac complications.

243
Q

What are the management options for Graves’ disease in adults, and what considerations should be made for each treatment?

A

–> ß-blockers:
Use: Control symptoms (e.g., palpitations).
Example: Propranolol.

–> Antithyroid Drugs:
First-line: Carbimazole or Propylthiouracil.
Duration: 12-18 months; used if remission is likely or other treatments are unsuitable.

Radioactive Iodine:
–> First-line: Preferred for most patients.
Avoid: Pregnancy, active eye disease, or malignancy concerns.
Surgery:

Indications: Compression, malignancy concerns, or if other treatments fail.

Risks: Potential nerve damage; may require replacement therapy.
Children/Young People: Antithyroid drugs for at least 2 years; refer to paediatric endocrinology.

Care Setting: Antithyroid drugs and ß-blockers can start in primary care; comprehensive management in secondary care.

244
Q

What is a key complication of carbimazole use?

A

Agranulocytosis

Phase 4 - Endo, Resp, Cardio, Haem, Opthal (5 decks)

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